There are two types of age-related macular degeneration (AMD): the dry (atrophic) form and the wet (exudative) form. The dry form of AMD affects about 90 percent of AMD patients and usually begins with the formation of tiny yellow deposits called drusen in the macula. Drusen usually do not cause serious loss of vision, but can cause distortion of vision. However, for reasons that are not yet understood, sometimes drusen will cause the macula to thin and break down, slowly leading to vision loss. The wet form of AMD occurs in about 10 percent of AMD patients. It is caused by the growth of abnormal blood vessels beneath the macula that can leak fluid and blood (i.e. exudate). The wet form of AMD typically causes significant vision problems in the affected eye and can progress very rapidly, causing permanent central vision loss. The exact cause of AMD is not known. AMD may be hereditary. Macular degeneration may never get better on its own.
Michael Schwartz (of the Weizmann Institute's Neurobiology Department) reports that capoxone may slow, or possibly stop the loss of eyesight in people with chronic glaucoma. Dr Schwartz's studies have shown that immunization with capoxone shields the optic nerve from the toxic effects of the neurotransmitter glutamate, which is released in increasing concentrations as the optic nerve degenerates. However, capoxone does not induce or stimulate the growth of new optic nerve fibers.
For the first time, researchers (a review article by Gary D. Vogin, MD in Medscape Medical News 2003. © 2003 Medscape) report that a pharmacologic intervention may effectively target the underlying abnormalities that lead to the development of type 2 diabetes. In a small pilot study in 11 patients with type 2 diabetes at an average age of 59 years (reported by Aaron I. Vinik, MD, PhD, director of the Strelitz Diabetes Research Institutes at Eastern Virginia Medical School in Norfolk, Va. at the American Diabetes Association 63rd Scientific Sessions, 2003), the anticonvulsant topiramate appeared to induce the growth of new nerve fibers and relieve symptoms of peripheral neuropathy while also improving components of metabolic syndrome. The patients were administered 25 mg/day, titrated over 42 days to the maximum tolerated dose or 100 mg/day. The patients received the anticonvulsant for 84 more days. By the end of trial, dendrite length and peroneal nerve amplitude had increased, and total neuropathy scores had decreased from 14 to 11.8. It suggests that intra-epidermal nerve fibers actually grew back and the nerve repairs itself. This provides the first opportunity to change the underlying biology of the disease as opposed to treating its symptoms. The above finding was presented at ADA 63rd Scientific Sessions: Abstract 66, presented Jun. 13, 2003, poster 1702, presented Jun. 14, 2003, entire contents of which are incorporated herein by reference.
U.S. Pat. No. 6,699,840, entire contents of which are incorporated herein by reference, discloses a controlled-release form of topiramate sodium trihydrate comprising topiramate sodium trihydrate and a means for controlled-release of the topiramate sodium trihydrate as a treatment method for symptoms.
U.S. Pat. No. 6,696,091, entire contents of which are incorporated herein by reference, discloses a pharmaceutical composition of topiramate as an anticonvulsant which is useful for treating epilepsy. More specifically, the invention provides a solid dosage formulation of topiramate intended primarily for use by pediatric patients, or for patients who have difficulty swallowing tablets. Processes for preparing the pharmaceutical composition are also described.
Clinical studies on topiramate have revealed previously unrecognized pharmacological properties which suggest that topiramate would be effective in lowering lipids in humans, particularly in overweight individuals. Furthermore, topiramate improves both symptoms and objective electrophysiological measurements of peripheral neuropathy while also lowering levels of total cholesterol, triglyceride, blood glucose, and blood pressure and promoting significant weight loss. Some aspects of the current invention provide a method of treating optic nerve degeneration comprising reducing optic nerve degeneration and/or inducing the growth of optic nerve fibers and/or stimulating functions of optic nerves.